Acute ischemic stroke remains the primary cause of disability worldwide. For patients with large vessel occlusions, intravenous thrombolysis followed by mechanical thrombectomy remains the standard of care. Revascularization of the large vessel is typically successful. However, despite reopening of the occluded vessel, many patients fail to return to independence. Functional failure, despite macrovascular recanalization, is often referred to as the no-reflow phenomenon. Even with an extensive characterization of reperfusion in animal models, numerous mechanisms may explain no-reflow. Further, uniform measurements of this microvascular dysfunction and prognostic markers associated with no-reflow are lacking. In this review, we highlight a number of mechanisms that may explain no-reflow, characterize current multimodal measurements, and assess its molecular markers.
Keywords: biomarkers; inflammation; reperfusion; thrombectomy; treatment.